假单胞菌效应蛋白HopB1通过破坏激活状态的免疫受体阻断植物免疫  

Activation-Dependent Destruction of a Co-receptor by a Pseudomonas syringae Effector Dampens Plant Immunity

作　　者：李磊 Panya Kim Liping Yu Gaihong Cai She Chen James R.Alfano 周俭民[3] 

机构地区：[1]德国马普发育生物学研究所 [2]不详 [3]中国科学院遗传与发育生物学研究所

出　　处：《科学新闻》2017年第4期101-101,共1页Science News

基　　金：国家自然科学基金;科技部;中国科学院先导专项等资金的资助

摘　　要：在植物和病原微生物互作过程中，植物通过不同的策略感受病原菌的侵染并激活免疫反应．从而抵抗病菌侵染。例如，植物细胞膜上存在一类免疫受体可以识别细菌保守的鞭毛蛋白来激活植物免疫反应。The Arabidopsis immune receptor FLS2 and co-receptor BAK1 perceive the bacterial flagellin epitope flg22 to activate plant immunity. To prevent this response, phytopathogenic bacteria deploy a repertoire of effector proteins to perturb immune signaling. However, the effector-induced perturbation is often sensed by the host, triggering another layer of immunity. We report that the Pseudomonas syringae effector HopB1 acts as a protease to cleave immune-activated BAK1. Prior to activation, HopB1 constitutively interacts with FLS2. Upon activation by flg22, BAK1 is recruited to the FLS2-HopB1 complex and is phosphorylated at Thr455. HopB1 then specifically cleaves BAK1 between Arg297 and Gly298 to inhibit FLS2 signaling. Although perturbation of BAK1 is known to trigger increased immune responses in plants, the HopB1-mediated cleavage of BAK1 leads to enhanced virulence, but not disease resistance. This study thus reveals a virulence strategy by which a pathogen effector attacks the plant immune system with minimal host perturbation.

关 键 词：免疫反应 植物 激活 受体 蛋白 状态 病原微生物 病原菌 

分 类 号：Q516[生物学—生物化学]